Generally, an erection is produced by a blood flow imbalance caused by increased arterial blood flow into the erectile tissues of the penis in the presence of restricted veinal blood flow from the penis. This imbalance enables the erectile tissue to become engorged with blood and causes penile enlargement or erection. The physiological events associated with the erectile process include a vascularization which increases arterial blood flow into the penis as well as a concurrent veno-constriction from the expanding cavernosa compression against the tunica, thereby causing an imbalance in blood flow rates to and from the penis. Erection persists as long as arterial inflow exceeds venous outflow.
The erectile process can fail for a number of reasons, resulting in any one of a number of erectile dysfunctions, including impotence. "Impotence" is the consistent inability to achieve or sustain an erection of sufficient rigidity for sexual intercourse. It has been estimated that approximately 10 million American men are impotent (R. Shabsigh et al., "Evaluation of Erectile Impotence," Urology 32:83-90 (1988); W. L. Furlow, "Prevalence of Impotence in the United States," Med. Aspects Hum. Sex. 19:13-16 (1985)). Impotence is recognized to be an age-dependent disorder, with an incidence of 1.9 percent at 40 years of age and 25 percent at 65 years of age (A. C. Kinsey et al., "Age and Sexual Outlet," in Sexual Behavior in the Human Male, A. C. Kinsey et al., eds., Philadelphia, Pa.: W. B. Saunders, 218-262 (1948)). In 1985 in the United States, impotence accounted for more than several hundred thousand outpatient visits to physicians (National Center for Health Statistics, National Hospital Discharge Survey, 1985, Bethesda, Md., Department of Health and Human Services, 1989 DHHS publication no. 87-1751).
A number of causes of impotence have been identified, including vasculogenic, neurogenic, endocrinologic and psychogenic. See Das, S., Int. J. Impotence Res. 6:183-189 (1984). Impotence may result from various physiological or psychological conditions which cause the blood flow rates to and from the penis to remain substantially in balance, thereby preventing the concomitant retention of blood in the penis, which is necessary to induce and maintain an erection. Impotence can also be a side effect of various classes of therapeutic drugs, or can be associated with various diseases, including diabetes, multiple sclerosis and sickle cell anemia. Impotence resulting from any one of these causes can be exacerbated by additional factors such as cigarette smoking, a poor diet, or the like.
A frequent physiological condition associated with impotence relates to "venous leakage" wherein the penile venous system is not sufficiently compressed during the erectile process, permitting excessive drainage of blood from penile tissue and subsequent detumescence or erectile failure. Diagnostic tests (e.g., cavernosography) have shown that upwards of 40% of impotent men suffer from some degree of venous leakage.
Numerous treatments for impotence are known in the art, and include psychological therapies, hormonal therapy, administration of various vasodilators, surgery (e.g., vascular surgery or implantation of penile prostheses), vacuum devices and various external aids such as penile splints and constriction devices. See e.g., Krane, et al., N. Eng. J. Med. 321(24):1648-1659 (1989). In light of the recognition that penile inflow arteries are principally within the deep interior of the organ, and that penile return veins are disposed both within the deep interior and subdermally, adjacent to the surface of the organ, a number of devices have been described wherein the blood flow from the penis may be restricted using external devices such as constriction bands. These devices are adapted to be placed about the penis at a location closely adjacent to the body trunk. Thus, the blood flow from the penis via the peripheral veins is impeded while the blood flow to the penis via the deeply embedded arteries remains substantially unimpeded, thereby assisting in the achievement and/or maintenance of an erection (Sidi et al., Urol. Clin. N. America, 17:19-21 (1990); U.S. Pat. Nos. 2,581,114 to Larson; 3,461,863 to Sullinger; 4,203,432 to Koch; 4,967,738 to March; 5,027,800 to Rowland).
More particularly, U.S. Pat. No. 2,581,114 to Larson describes a constriction device consisting of an elongated elastic tube with a rigid U-shaped yoke which provides the "socket" of a ball-and-socket coupling means for fastening the device in place about a penis, and impeding venous outflow. U.S. Pat. No. 3,461,863 to Sullinger describes an adjustable constriction device consisting of a loop of flexible tubing having two apertures arranged at one end of the tubing which allow the other end to pass through and provide a means for fastening the device in place. Sullinger further describes the importance of the relative spacing of the two apertures and tube wall thickness to prevent or resist slippage of the device in response to increased tension. Sidi et al. describe a multi-component tourniquet device comprised of flexible tubing, an associated elongate locking mechanism, and a separate release loop. The flexible tubing is routed through a first aperture in the locking mechanism, doubled back to form a loop, and routed through a second aperture in the locking mechanism. The device is described for use in conjunction with the intracavernosal administration of drugs in the diagnosis and treatment of impotence.
Although these devices, as well as other types of constriction or clamping devices known in the art, are capable of restricting blood flow from the penis, these devices are subject to several disadvantages in the treatment or prevention of erectile failure. One common disadvantage involves a lack of a means to adjust constrictive tension, rendering it difficult or impossible to control the degree of veinal outflow restriction necessary to prevent erectile failure. Insufficient restriction may prevent such devices from maintaining an erection, and too much restriction may result in user discomfort, numbness and insensitivity, and may even result in damage to the penile tissue if left in place for an extended period of time. Prior devices which may exert excessive constriction can cause substantial or complete restriction of arterial blood flow into the penis, resulting in serious injury. Further, since the degree of veinal restriction provided by prior devices depends in part on the stage of the individual's erection, a problem arises when such devices are adjusted to a particular tightness suitable for achieving an initial erection that subsequently becomes too restrictive thereafter.
Other approaches to inducing erection and preventing erectile failure include physiological treatments such as injection of a vasoactive drug directly into a corpora cavernosa. See, for example, U.S. Pat. Nos. 4,127,118 to Latorre, 4,766,889 to Trick et al., and 4,857,059 to Rey et al. Commonly used drugs include .alpha.-adrenergic blocking agents such as the long acting phenoxybenzamine and the short acting phentolamine, smooth muscle relaxants such as papaverine, prostaglandins having vasoactive function such as prostaglandin-E.sub.1 (PGE.sub.1) and combinations thereof. See Kursh et al., Urol. Clin. of No. America 15(4):625-629 (1988), and Ishii et al., J. of Urol. 141:323-325 (1989). Yet another approach involves topical application of an agent such as a vasodilator directly to the various skins or mucosa of the penis. Commonly used agents include hydralazine, sodium nitroprusside, phenoxybenzamine and phentolamine (see U.S. Pat. No. 4,801,587 to Voss et al.). Although such therapies provide sufficient prevention of erectile failure in some individuals, loss of erection upon lying down or incomplete response to the vasoactive drugs at high dosages may be manifestations of excessive venous outflow from the penis. In such instances, the concurrent use of a venous outflow control device may be indicated.
Accordingly, there remains a need for a therapeutic device adapted for application to the penis that is useful to treat or prevent erectile failure. Such a device must be capable of providing readily adjustable control over venous outflow, whereby proper use thereof enhances retention of blood within an individual's penis without substantially obstructing arterial inflow or becoming too constrictive during the erectile process. Further, there remains a need for a venous flow control device which may be employed to supplement or improve the efficacy of physiological treatments for erectile failure, such as in the therapeutic administration of vasoactive or androgenic agents and the like. The devices may be used to reduce the required dosage, and/or to render effective a dosage which is ineffective in the absence of the device. That is, the administered agent remains within the penis for an extended period of time, and enhances the effectiveness of the drug therapy. It is also desirable that any such device be simple in structure, so as to provide ease and economy of manufacture.